The gastrointestinal tract is a dynamic interactive barrier that normally segregates microbial populations from their cognate human hosts. An aberrant consequence of contact between microbes and gut epithelial cells is the development of mucosal inflammation, which, if allowed to become persistent, can initiate carcinogenic pathways. Gastric adenocarcinoma is the second leading cause of cancer-related death in the world, and Helicobacter pylori, a bacterial species that persistently colonizes the human stomach and induces chronic gastritis, is the strongest known risk factor for this malignancy. However, only a fraction of infected persons ever develop cancer, underscoring the importance of defining mechanisms that regulate the biological interactions of H. pylori with their hosts that promote neoplastic transformation. Adherence of H. pylori to gastric epithelial cells is critical for induction of inflammation and injury; therefore, the overarching theme for our research has been delineation of the molecular signaling events initiated by bacterial:epithelial cell contact that regulate phenotypes related to carcinogenesis.